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Publicly Available Published by De Gruyter July 1, 2016

Effect of conditioned pain modulation on long-term potentiation-like pain amplification in humans

  • Weiwei Xia EMAIL logo , Carsten Dahl Mørch , Dagfinn Matre and Ole Kæseler Andersen

Abstract

Aim

The current study aimed to explore the effect of conditioned pain modulation (CPM) on the long-term potentiation (LTP)-like pain amplification induced by peripheral 10 Hz conditioning electrical stimulation (CES).

Methods

Sensory changes and neurogenic inflammatory vas-cular reactions induced by 10 Hz CES were assessed in twenty subjects in a randomized crossover design involving two experimental days separated by at least one week. The CPM effect was activated by cold pressor test (CPT) (4 °C) which was applied immediately before the 10 Hz CES in the active session and 32 °C water was used in the control session. Perceptual intensity ratings to single electrical stimulation (SES) at the conditioned skin site and to mechanical stimuli (pinprick and light stroking) in the immediate vicinity of the electrode for CES were recorded. Superficial blood flow (SBF), skin temperature (ST), and heat pain threshold (HPT) were also measured. The pain intensities during the CES process were recorded and the short-form McGill Pain Questionnaire (SF-MPQ) was used for assessing the pain experience.

Results

CPT reduced the pain perception increments to pin-prick (12.8 g) and light stroking stimuli after 10 Hz CES compared to the control session. Moreover, CPT resulted in lower pain intensity ratings during the CES process but without significant changes in the SF-MPQ scores between the two sessions. The SBF and ST were found to increase after CES and then gradually decline but without differences between the CPT and the control sessions. No CPM effect was found for HPT and pain intensity increments to SES.

Conclusions

The cold pressor test inhibited heterotopic perception amplification to mechanical stimuli after conditioning electrical stimulation. The results indicate that endogenous descending inhibitory systems may affect pain-amplificatory mechanisms.

Published Online: 2016-07-01
Published in Print: 2016-07-01

© 2016 Scandinavian Association for the Study of Pain

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